We are analyzing https://link.springer.com/article/10.1007/s40495-018-0141-6.

Title:
Histone H3 Mutations in Cancer | Current Pharmacology Reports
Description:
Histone modifications are one form of epigenetic information that relate closely to gene regulation. Aberrant histone methylation caused by alteration in chromatin-modifying enzymes has long been implicated in cancers. More recently, recurrent histone mutations have been identified in multiple cancers and have been shown to impede histone methylation. All three histone mutations (H3K27M, H3K36M, and H3G34V/R) identified result in amino acid substitution at/near a lysine residue that is a target of methylation. In the cases of H3K27M and H3K36M, found in pediatric DIPG (diffuse intrinsic pontine glioma) and chondroblastoma respectively, expression of the mutant histone leads to global reduction of histone methylation at the respective lysine residue. These mutant histones are termed “oncohistones” because their expression reprograms the epigenome and shapes an oncogenic transcriptome. Dissecting the mechanism of H3K27M-driven oncogenesis has led to the discovery of promising therapeutic targets in pediatric DIPG. The purpose of this review is to summarize the work done on identifying and dissecting the oncogenic properties of histone H3 mutations.
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Keywords {🔍}

hkm, pubmed, histone, article, hkme, google, scholar, cas, mutations, cell, central, cells, genes, dipg, prc, cancer, glioma, gene, methylation, found, pediatric, expression, loss, cancers, hkac, reported, tumor, ezh, nat, diffuse, mutation, group, gain, inhibition, lysine, intrinsic, pontine, targets, nature, analysis, modifications, oncohistones, oncogenesis, therapeutic, tumors, polycomb, activity, identified, regions, model,

Topics {✒️}

nsd1/nsd2/setd2 triple knockdown article download pdf gov/pubmed/28067913 http integrated molecular meta-analysis kui ming chan pediatric high-grade glioma brainstem high-grade glioma epigenetics search search open access published h3k27m-mutant pediatric gliomas h3 wild-type mouse tumor type-specific occurrence h3k36me3-deficent u2os cells cell type-independent phenomenon g34v/r-gbm cells wild-type h3 peptide mek/erk pathways showed anti-tumor activity histone tail modifications histone modifications include 000 pediatric high-grade gene ontology analysis h3k36m-expressing murine mpc article wan chip-seq analysis clinically distinct group h3k36me3-deficient cells h3-wt nucleosome reduced somatic genomic landscape long-term gene repression polypeptide-related sequence aberrant histone modifications recurrent somatic mutations full access related subjects privacy choices/manage cookies showed reduced growth animal subjects performed p16-independent oncogenic pathway springer berlin heidelberg taylor kr nat rev cancer mesenchymal stem cells renal cell cancer h3k27m-driven oncogenic mechanism prc2-mediated gene repression nat publ group dipg cell lines tumor type-specific gskj4-treated cells

Questions {❓}

3K27M mutation found in pediatric glioma A new approach to the study of the function of histone modifications in vivo?
Could this point to the existence of the corresponding histone mutations?
Paediatric and adult malignant glioma: Close relatives or distant cousins?

Schema {🗺️}

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         headline:Histone H3 Mutations in Cancer
         description:Histone modifications are one form of epigenetic information that relate closely to gene regulation. Aberrant histone methylation caused by alteration in chromatin-modifying enzymes has long been implicated in cancers. More recently, recurrent histone mutations have been identified in multiple cancers and have been shown to impede histone methylation. All three histone mutations (H3K27M, H3K36M, and H3G34V/R) identified result in amino acid substitution at/near a lysine residue that is a target of methylation. In the cases of H3K27M and H3K36M, found in pediatric DIPG (diffuse intrinsic pontine glioma) and chondroblastoma respectively, expression of the mutant histone leads to global reduction of histone methylation at the respective lysine residue. These mutant histones are termed “oncohistones” because their expression reprograms the epigenome and shapes an oncogenic transcriptome. Dissecting the mechanism of H3K27M-driven oncogenesis has led to the discovery of promising therapeutic targets in pediatric DIPG. The purpose of this review is to summarize the work done on identifying and dissecting the oncogenic properties of histone H3 mutations.
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      headline:Histone H3 Mutations in Cancer
      description:Histone modifications are one form of epigenetic information that relate closely to gene regulation. Aberrant histone methylation caused by alteration in chromatin-modifying enzymes has long been implicated in cancers. More recently, recurrent histone mutations have been identified in multiple cancers and have been shown to impede histone methylation. All three histone mutations (H3K27M, H3K36M, and H3G34V/R) identified result in amino acid substitution at/near a lysine residue that is a target of methylation. In the cases of H3K27M and H3K36M, found in pediatric DIPG (diffuse intrinsic pontine glioma) and chondroblastoma respectively, expression of the mutant histone leads to global reduction of histone methylation at the respective lysine residue. These mutant histones are termed “oncohistones” because their expression reprograms the epigenome and shapes an oncogenic transcriptome. Dissecting the mechanism of H3K27M-driven oncogenesis has led to the discovery of promising therapeutic targets in pediatric DIPG. The purpose of this review is to summarize the work done on identifying and dissecting the oncogenic properties of histone H3 mutations.
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         Cancer Research
         Molecular Medicine
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      name:Key Laboratory of Biochip Technology, Biotech and Health Centre, Shenzhen Research Institute of City University of Hong Kong, Shenzhen, China
      name:Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China
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